Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, also known as disorders of the gut–brain interaction; however, the pathophysiology of IBS remains unclear. Early life stress (ELS) is one of the most common risk factors for IBS development. However, the molecular mechanisms by which ELS induces IBS remain unclear. Enterochromaffin cells (ECs), as a prime source of peripheral serotonin (5-HT), play a pivotal role in intestinal motility, secretion, proinflammatory and anti-inflammatory effects, and visceral sensation. ECs can sense various stimuli and microbiota metabolites such as short-chain fatty acids (SCFAs) and secondary bile acids. ECs can sense the luminal environment and transmit signals to the brain via exogenous vagal and spinal nerve afferents. Increasing evidence suggests that an ECs-5-HT signaling imbalance plays a crucial role in the pathogenesis of ELS-induced IBS. A recent study using a maternal separation (MS) animal model mimicking ELS showed that MS induced expansion of intestinal stem cells and their differentiation toward secretory lineages, including ECs, leading to ECs hyperplasia, increased 5-HT production, and visceral hyperalgesia. This suggests that ELS-induced IBS may be associated with increased ECs-5-HT signaling. Furthermore, ECs are closely related to corticotropin-releasing hormone, mast cells, neuron growth factor, bile acids, and SCFAs, all of which contribute to the pathogenesis of IBS. Collectively, ECs may play a role in the pathogenesis of ELS-induced IBS. Therefore, this review summarizes the physiological function of ECs and focuses on their potential role in the pathogenesis of IBS based on clinical and pre-clinical evidence.

Kawasaki disease (KD) is an acute febrile multisystem vasculitis and has been recognized to be one of the most common causes of acquired heart disease in children. Although gastrointestinal symptoms including vomiting, diarrhea, and abdominal pain are not uncommon in KD patients, KD with lower gastrointestinal bleeding is quite rare. Here, we describe a 3-year-old boy with typical KD who had lower gastrointestinal bleeding caused by rectal ulcers on the third day of aspirin therapy.

Background Kawasaki disease (KD) is an acute febrile multisystem vasculitis and has been recognized to be the most common cause of acquired heart disease in children. Owing to its propensity to involve vessels throughout the entire body, KD often mimics other disease processes. The diagnosis might be delayed if other prominent symptoms appear before the characteristic clinical features of KD. Although gastrointestinal symptoms including vomiting, diarrhea, and abdominal pain are not uncommon in KD patients, KD with gastrointestinal bleeding is quite rare. Case presentation A previously healthy 4-year-old boy initially presented with abdominal pain, followed by fever, rash, and gastrointestinal hemorrhage, eventually diagnosed as complete KD. The patient recovered smoothly after appropriate management and no subsequent complications occurred in the following months. Conclusion The diagnosis of KD should be considered in children presenting with abdominal symptoms and fever without definable cause. Pediatricians should be aware of the risk of gastrointestinal bleeding in patients with KD, especially in those with prominent abdominal symptoms.

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(1) Background: Irritable bowel syndrome (IBS) is a global public health problem, the pathogenesis of which has not been fully explored. Limiting fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) can relieve symptoms in some patients with IBS. Studies have shown that normal microcirculation perfusion is necessary to maintain the primary function of the gastrointestinal system. Here, we hypothesized that IBS pathogenesis might be related to abnormalities in colonic microcirculation. A low-FODMAP diet could alleviate visceral hypersensitivity (VH) by improving colonic microcirculation; (2) Methods: C57BL/6 mice were raised to establish an IBS-like rodent model using water avoidance (WA) stress or SHAM-WA as a control, one hour per day for ten days. The mice in the WA group were administered different levels of the FODMAP diet: 2.1% regular FODMAP (WA-RF), 10% high FODMAP diet (WA-HF), 5% medium FODMAP diet (WA-MF), and 0% low FODMAP diet (WA-LF) for the following 14 days. The body weight and food consumption of the mice were recorded. Visceral sensitivity was measured as colorectal distention (CRD) using the abdominal withdrawal reflex (AWR) score. Colonic microcirculation was assessed using laser speckle contrast imaging (LCSI). Vascular endothelial-derived growth factor (VEGF) was detected using immunofluorescence staining; (3) Results: The threshold values of CRD pressure in the WA-RF, WA-HF, and WA-MF groups were significantly lower than those in the SHAM-WA group. Moreover, we observed that colonic microcirculation perfusion decreased, and the expression of VEGF protein increased in these three groups of mice. Interestingly, a low-FODMAP dietary intervention could reverse this situation. Specifically, a low-FODMAP diet increased colonic microcirculation perfusion, reduced VEGF protein expression in mice, and increased the threshold of VH. There was a significant positive correlation between colonic microcirculation and threshold for VH; (4) Conclusions: These results demonstrate that a low-FODMAP diet can alter VH by affecting colonic microcirculation. Changes in intestinal microcirculation may be related to VEGF expression.

We assessed dynamic changes in visceral hypersensitivity and fecal metabolomics through a mouse model of irritable bowel syndrome (IBS) from childhood to adulthood. A mouse model of IBS was constructed with maternal separation (MS) in early life. Male mice aged 25, 40, and 70 days were used. Visceral sensitivity was assessed by recording the reaction between the abdominal withdrawal reflex and colorectal distension. Metabolomics was identified and quantified by liquid chromatography-tandem mass spectrometry. The visceral sensitivity of the MS group was significantly higher than that of the non-separation (NS) group in the three age groups. The top four fecal differential metabolites in the different age groups were lipids, lipid molecules, organic heterocyclic compounds, organic acids and derivatives, and benzenoids. Five identical differential metabolites were detected in the feces and ileal contents of the MS and NS groups at different ages, namely, benzamide, taurine, acetyl-L-carnitine, indole, and ethylbenzene. Taurine and hypotaurine metabolism were the most relevant pathways at P25, whereas histidine metabolism was the most relevant pathway at P40 and P70. Visceral hypersensitivity in the MS group lasted from childhood to adulthood. The different metabolites and metabolic pathways detected in MS groups of different ages provide a theoretical basis for IBS pathogenesis.

Aim: We aim to investigate the endoscopic and CT scan findings of pediatric patients with Henoch-Schonlein purpura (HSP). Methods: The endoscopic and CT findings of the patients were observed. Endoscopy was carried out using the Olympus GIF XQ 230 electronic gastroscope. Laboratory tests were carried out to investigate the expression of potential markers in these patients. In total, 4 females and 2 males were included in this study, with the median age of 7.5 yrs. All the 6 patients underwent endoscopic examination. Results: One showed hyperemia and erosion in the gastric antrum, together with punctiform hyperemia in the gastric balloon and bile regurgitation. One showed erosion in the gastric fundus, body and angle, as well as hyperemia and edema in the descendant duodenum, together with massive erosion and ulcer. One showed hyperemia and erosion in the gastric antrum combined with ecchymosis in the descending part of stomach. One showed ecchymosis in the descendant duodenum, and a tendency of hemorrhage. One showed massive ecchymosis in the descendant part and horizontal part of the duodenum. The other one showed hyperemia in the descendant duodenum. Endoscopic findings of HSP consisted of mucous hyperemia and edema, together with local erosion and irregular ulcer. Some patients at the acute stage presented hemorrhagic spots and capillary hemorrhage, which usually involved the duodenum, gastric antrum and body. Conclusion: CT findings of the HSP were edema and thickening in the small intestinal wall, hydrops in the intestinal cavity and intestinal obstruction.